期刊
FRONTIERS IN PHARMACOLOGY
卷 12, 期 -, 页码 -出版社
FRONTIERS MEDIA SA
DOI: 10.3389/fphar.2021.651582
关键词
hypertension; hyperhomocysteinemia; folate; oxidative stress; arterial inflammation
资金
- Shandong Provincial Key Research and Development Programme Foundation, China [2018GSF118009]
- Technology Programme Foundation of Jinan, China [201821007]
- Shandong Provincial Medical Science and Technology Development Programme Foundation, China [2017WS462]
- Jinan City Medical and Health Development Plan [2018-2-31]
This study found that HHcy synergistically aggravated arterial damage in hypertensive rats through immune/inflammatory response, while folate demonstrated anti-inflammatory properties and reversed the NF-kappa B p65/Rela/IL-6 levels induced by HHcy.
Hyperhomocysteinemia (HHcy) is derived from the abnormal metabolism of homocysteine (Hcy) and is related to metabolic-related diseases. In addition, HHcy combined with hypertension increases the risk of cardiovascular diseases (CVD). However, the mechanism of HHcy aggravating hypertensive arterial damage and the efficacy of folate (FA) as a beneficial supplement have not been fully elucidated. In this study, we established a rat HHcy model and a hypertension combined with HHcy model. Rat tail artery blood pressure (BP), plasma Hcy, serum superoxide dismutase (SOD), and malondialdehyde (MDA) were measured. Rat thoracic aorta was for pathological analysis after 12 weeks of the experiment. The relative expression levels of oxidative stress and immune/inflammation in rat arterial tissues were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blotting. The results demonstrated that the relative expression levels of oxidative stress and immune/inflammation were the highest in the hypertension combined with HHcy group, followed by the hypertension group. Compared with the hypertension group, the hypertension combined with HHcy group up-regulated the expression levels of interleukin-6 (IL-6) and nuclear factor-kappa-gene binding (NF-kappa B) p65/Rela, but not NADPH oxidase (Nox). Furthermore, folate inhibited the expression of IL-6 and NF-kappa B p65/Rela, reduced the levels of MDA and HHcy, but significantly increased the SOD level. In conclusion, HHcy synergistically aggravated the arterial damage factor of hypertension through immune/inflammatory response. However, folate demonstrated anti-inflammatory properties and reversed the NF-kappa B p65/Rela/IL-6 level induced by HHcy in hypertensive rats.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据